formation of urine 2 Flashcards
What is extracted in the descending limb
Water
What is extracted in the ascending limb
Na+ and Cl-
Thin descending limb
No active transport of salts
Freely permeable to water AQP 1
Passive movement of water via tight junctions
Thick ascending limb
Impermeable to water
NKCC2 co transporters - these ions reabsorbed
Loop of Henle
Filtrate is hypertonic at the tip of the LOH
Solutes are pumped out of ascending LOH
At end of LOH, filtrate entering the distal tubule is hypotonic
Countercurrent multiplication
Creates large osmotic gradient within medulla - Na+/K+/Cl- transport in ascending limb
Permits passive reabsorption of water from tubular fluid in descending limb
Urea reabsorption
LOH and distal tubule impermeable to urea (some absorption at proximal tubule)
Urea can diffuse out the collecting duct into medulla - adds to osmolality of medullary interstitial
Absorption in the distal tubule
Na+ and Cl- actively reabsorbed from tubular fluid in exchange for K+ or H+ (secreted into tubular fluid)
This involves principal cells (sensitive to aldosterone)
10-15% water reabsorbed
Where is Na+ exchanged for K+
Late DT and early collecting duct
Where is Na+ exchanged for H+
DT and early collecting duct
Involves alpha and beta intercalated cells
Alpha intercalated cells
Secretes acid (H+/Na+ or H+/K+) Reabsorbs bicarbonate
Beta intercalated cells
Secrete bicarbonate
Reabsorbs acid
ADH mechanism & action
Released from posterior pituitary subsequent to hypothalamic inputs
Plasma half life: 10-15 mins
Acts on vasopressin V2 receptors on basal membrane of principal cells in DT -> activation of AQP2
Max vs min ADH
Max = 66% reabsorption
Urine volume reduced to 300mL/day
Min/none: impermeable collecting duct wall (30L/day excretion)
Lack of ADH: diabetes insipidus
Diabetes insipidus - 2 types
Nephrogenic - kidneys can’t respond to ADH - treatment diuretic/anti-inflammatory
Neurogenic - lack of production - ADH analogue/anti-convulsive
